The long-range goal of this study is to analyze the significance of selected biochemical alterations of cancer cells in a well-defined model of pancreatic acinar cell carcinoma and to gain further insight into the mechanisms underlying aberrant behavior of neoplastic cells. As a part of our broader investigation on the pathogenesis of acinar cell carcinoma of the pancreas in experimental animals, we recently established cultures of acinar cells derived from chemically induced rat pancreatic carcinoma and maintained those cells as subcutaneous tumors on nude mice. Preliminary studies have revealed a number of alterations in glycoprotein and lipid metabolism of these tumors. Using both the fast and slow growing cancer cells in culture and their corresponding transplantable tumors on nude mice, we have demonstrated: (1)\enhanced cholesterol levels; (2)\enhanced HMGCoA reductase activity; (3)\loss in the feedback inhibition of de novo synthesis of cholesterol; and (4)\a shift from high to low molecular weight glycoproteins. In this investigation we propose to extend our study on the interrelationships between cholesterol and glycoprotein metabolism in pancreatic acinar cell carcinomas and test the hypothesis that "a defect in the receptor mediated uptake of low density lipoproteins (LDL) leads to loss in the feedback inhibition of de novo synthesis of cholesterol and high activity in the tumor cell populations." Specifically, we wish to study the receptor-mediated uptake of LDL in the fast and slow growing pancreatic acinar cell carcinomas and elucidate the mechanisms underlying differences in receptor-mediated uptake of LDL between the two tumors by analyzing synthesis and degradation of their LDL receptors.